Chondroitin polymerizing factor (CHPF) has been reported to play a pivotal role in the progression of multiple cancers, however, the relationship between CHPF and colorectal cancer (CRC) progression has not been fully understood. The current study revealed that CHPF expression was upregulated in patients with CRC and correlated with an unfavorable prognosis. Also, CHPF knockdown effectively suppressed the viability and mobility of CRC cells and the growth of xenograft tumors. Additionally, SMAD9 was identified as a downstream target of CHPF. SMAD9 knockdown successfully abrogated the promotion of CHPF overexpression in CRC progression, indicating that CHPF regulated the development of CRC through SMAD9. Mechanistically, SMAD9 is ubiquitinated by ASB2, and the regulatory effect of CHPF on SMAD9 activity was exerted via its mediation of ASB2. Collectively, CHPF functioned as a promising prognostic biomarker and tumor-promoter of CRC by regulating the ASB2-mediated ubiquitination of SMAD9.

中文翻译：

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软骨素聚合因子 (CHPF) 通过 ASB2 介导的 SMAD9 泛素化促进结直肠癌的进展。

据报道，软骨素聚合因子（CHPF）在多种癌症的进展中发挥着关键作用，然而，CHPF 与结直肠癌（CRC）进展之间的关系尚未完全了解。目前的研究表明，CRC 患者中 CHPF 表达上调，并与不良预后相关。此外，CHPF 敲低有效抑制了 CRC 细胞的活力和迁移性以及异种移植肿瘤的生长。此外，SMAD9 被确定为 CHPF 的下游靶标。 SMAD9敲低成功消除了CHPF过表达对CRC进展的促进作用，表明CHPF通过SMAD9调节CRC的发展。从机制上来说，SMAD9被ASB2泛素化，CHPF对SMAD9活性的调节作用是通过其介导ASB2来发挥的。总的来说，CHPF 通过调节 ASB2 介导的 SMAD9 泛素化而发挥着有前景的 CRC 预后生物标志物和肿瘤促进剂的作用。